Transcript 18 The Somatosensory System II: Touch, Thermal Sense, and …

18 The Somatosensory System
II: Touch, Thermal Sense, and
Pain
Suhail Abdulla AlRukn
18-3-2008
Out-line
•
•
•
•
•
•
Objective
Test
Main Sensory Pathway
Sensory dysfunction
Anterolateral System
Peripheral Sensitization and Central
Sensitization
• Spinal Trigeminal Pathway
Objectives
• Define the main pathway for the
– Anterolateral pathway
– Spinal Trigeminal Pathway
• The mechanism of peripheral Vs
centrat sensitisation
Test
• What are the main sensory pathways
(body and face), what function, and where
it cross?
Main Sensory Pathway
Posterior
Vib, joint
Column-madial position, fine
lemniscal
touch
pathway
Internal arcuate
fibers (lower
medulla)
Anterolateral
pathway
Anterior
commissure
(spinal cord)
Pain, Temp,
crude touch
• Anterolateral system (ALS):
– Crude touch
– Thermal sanitation
– Pain
Trunk, limbs,
back of the
head
• Anterior Trigeminothalamic pathway (Spinal
Trigeminal Pathway):
– Crude touch
– Thermal sanitation
– Pain
Face and from
of the head
Anterolateral
system and
anterior
trigeminothalamic
Pathway
ALS Vs post. Colum pathways:
(1) Generalized feeling of being touched
but do not give precise localization,
(2) Receptive fields are larger,
(3) Fibres are smaller in diameter and
more slowly conducting.
Peripheral Sensory and Motor Fibers: Groups,
Diameters, and Conduction Velocities
Electrophysiol
ogic
Classification
of Peripheral
Nerves
Classification of
Afferent Fibers ONLY
(Class/Group)
Fiber
Diameter
(μm)
Conduction
Velocity
(m/s)
Receptor
Supplied
Sensory Fiber Type
Aα
Ia and Ib
13-20
80-120
Aβ
II
6-12
35-75
Aδ
III
1-5
5-30
Skin
mechanoreceptors,
thermal receptors, and
nociceptors
C
IV
0.2-1.5
0.5-2
Skin
mechanoreceptors,
thermal receptors, and
nociceptors
Primary muscle
spindles, Golgi tendon
organ
Secondary muscle
spindles, skin
mechanoreceptors
Sensory dysfunction
• Hypesthesia: reduced sensibility,
• Paresthesia: numbness, tingling, and prickling,
• Anesthesia loss of sensibility.
• Allodynia: an innocuous stimulus will result in a
perception of pain in the absence of a proper pain
stimulus.
• Hyperalgesia: is a heightened sensitivity to
painful stimuli
Anterolateral System
•
•
•
•
•
spinothalamic fibers
spinomesencephalic fibers
spinoreticular fibers
spinobulbar fibers
spinohypothalamic fibers
Anterolateral System
• Spinothalamic fibers project directly from
the spinal cord to the ventral posterolateral
(VPL) nucleus
• Spinomesencephalic axons project to the
periaqueductal area and to the tectum; the
latter are spinotectal fibers. Play role in
central modulaton of pain.
• Spinoreticular tract: carried the emotional
and arousal aspect of pain.
Figure 18-1 Summary
of anterolateral
system and anterior
trigeminothalamic
tract fibers
conveying
nondiscriminative
tactile, thermal, and
nociceptive inputs to
the contralateral
somatosensory
cortex.
Figure 18-1 Summary
of anterolateral
system and anterior
trigeminothalamic
tract fibers
conveying
nondiscriminative
tactile, thermal, and
nociceptive inputs to
the contralateral
somatosensory
cortex.
To summarize
• If you step on a sharp object with your left foot,
your spinothalamic tract enables you to realize
“something sharp is puncturing the sole of my
left foot”.
• Your spinothalamic intralaminar projections and
spinoreticular tract cause you to feel “ouch, that
hurts!”;
• And your spinomesencephalic tract leads to pain
modulation, allowing you eventually to think
“aah, that feels better”.
Peripheral Sensitization and
Primary Hyperalgesia
• Following an insult,
– pain receptors become more sensitive
– lower pain threshold
– increases in firing rate to noxious stimulation.
• So there will be increase in spontaneous activity
in the Aδ and C fibers.
• Although the mechanisms responsible for
receptor sensitization are not completely known,
chemicals released by the damaged skin or by
products from plasma, or both, are thought to
contribute to this phenomenon.
Peripheral Sensitization and
Primary Hyperalgesia
• As a result of this heightened sensitivity, the
affected area is super-sensitive to painful stimuli
and patients experience hyperalgesia.
• Primary hyperalgesia: occurs in the region of
damaged skin and is probably the result of
receptor sensitization.
• An example of primary hyperalgesia is the extreme
sensitivity of sunburned skin, which results from
sensitization of the skin pain endings by local tissue
products from the burn-perhaps histamine,
prostaglandins, and others
Central Sensitization and
Secondary Hyperalgesia
• Secondary hyperalgesia occurs in the skin
bordering the damaged tissue. Although
receptor sensitization may contribute to
secondary hyperalgesia, there is likely to be
a central (e.g., spinal) component as well.
• There is hyper-activation of the cell in the
posterior horn.
Central Sensitization and
Secondary Hyperalgesia
• This could be explain by:
– increase in the receptive field size of the posterior
horn neuron
– an increased response of the cells to the
application of suprathreshold stimuli,
• This phenomenon is known as central
sensitization, and it represents a potentiated
state in which the system has been shifted
from one functional level (normal) to another
(sensitized) by a change in transcription.
Pain Receptors in Muscles, Joints,
and Viscera
• In addition to the cutaneous pain receptors, pain
receptors in muscles, joints, and viscera have
also been identified, which are also carried by III
and IV afferent fibers type.
• A pinprick exam usually activates Aδ fibers.
• Dull, persistent ache that follows a muscle pull
results from activation of C fibers.
Dermatom of
the body
and face
Central Pathways
• Aδ and C fibers enter the spinal cord via
the lateral division of the posterior root
entry zone. The fibers enter the
posterolateral fasciculus (Lissauer tract)
and bifurcate into ascending and
descending branches
Summary of posterior horn laminae and their major sensory inputs (A) and major outputs (B).
Central Pathways
• When Aδ fibers enter the posterolateral
fasciculus and bifurcate, their branches
travel rostrocaudally for three to five spinal
levels.
• The descending branches terminate on
interneurons within the spinal gray that
participate in segmental spinal reflexes.
The general somatotopic arrangement of the anterolateral system
Somatotopically Arrange
DCT
CST
ALS
ARM
Trunk
LEG
• The ascending branches terminate on secondorder neurons (tract cells) in lamina I of the
posterior horn (Fig. 18-7A). These tract cells, in
turn, project to the thalamus.
• The great majority of their axons cross the
midline of the spinal cord obliquely via the
anterior (ventral) white commissure and ascend
in the contralateral ALS.
• A few ascend in the ipsilateral ALS.
• The thalamic (third-order) neurons of these
pathways are located mainly in the VPL, the
posterior nucleus, and the intralaminar nuclei.
The
anterolateral
system
Blood supply to
the anterolateral
system in the
spinal cord and
medulla
Brown-Séquard syndrome
• (1) contralateral loss of pain and thermal
sensations over the body below the level
of the lesion
• (2) ipsilateral loss of discriminative tactile,
vibratory, and position sense over the
body below the level of the lesion
• (3) ipsilateral paralysis of the leg or leg
and arm, depending on the level of the
hemisection.
Brown-Séquard syndrome
Cervical syringomyelia
Summary of the
spinocervicothala
mic tract that
carries innocuous
discriminative
tactile, thermal,
and nociceptive
sensations.
Spinal Trigeminal Pathway:
Anterior Trigeminothalamic Tract
Spinal Trigeminal Pathway:
Anterior Trigeminothalamic Tract
• Cranial nerves V, VII, IX, and X serve the
cutaneous receptors of the face, the oral cavity.
• The primary sensory fibers of these nerves have
their cell bodies in the:
– Trigeminal ganglion,
– Geniculate ganglion of cranial nerve VII,
– Superior ganglia of cranial nerves IX and X.
Anterior Trigeminothalamic Tract
• Aδ and C fiber are found throughout the
face and oral cavity.
• The meninges are also supplied by fibers
of the trigeminal ganglion cells that
terminate in the spinal trigeminal nucleus.
Trigeminal sensory nucleus
• Mesencephalic trigeminal nucleus
• Propriception
• Chief trigeminal nucleus
• Fine touch
• Spinal trigeminal nucleus
• Pain, temp, crude touch
Trigeminal
lemniscus Tract
Anterior
Trigeminothalamic
Tract
The spinal trigeminal nucleus
• Divided into:
–pars caudalis,
• nondiscriminative touch, pain, and thermal
sensations.
–pars interpolaris,
–pars oralis.
Pars caudalis
cross section
Trigeminal nerve
distribution
Lateral medullary (Wallenberg)
syndrome.
Dysfunction
Effects
Lateral soinothalamic Tract
Contralateral deficits in pain and
temperature sensation from body
Spinal Thalamic Nucleus
Ipsilateral loss of touch pain and
temperature sensation from face
Nucleus Ambiguus (which affects X and
nerves IX)
Dysphagia, horseness, diminished
gag reflex
Vestibular system
Vertigo, nystagmus, vomiting
descending sympathetic fibers
ipsilateral Horner’s syndrome
Centarl Tegmental Tract
Palatal myoclonus
Inferior Cerebellar Peduncle
Ipsilateral cerebellar signs including
ataxia
Chronic pain
Thalamic lesioning
• Lateral thalamic lesions involve: VPL/VPM.
– pain relief
– S/E: loss of cutaneous and position sense in the
affected limb, impaired motor function.
• Medial thalamus lesion involve: the centromedianparafascicular complex CM-PF, the central lateral
nucleus, the medial dorsal nucleus.
– Pain relief.
– Less S/E
Chronic pain
• Deep brain stimulation.
– Stimulating electrodes centered in the
somatosensory thalamus, the CM-PF
complex, or the periventricular gray (PVG)PAG activate neurons.
Questions
Test
• What are the nucleus:
– Mesencephalic trigeminal nucleus
• Propriception
– Chief trigeminal nucleus
• Fine touch
– Spinal trigeminal nucleus
• Pain, temp, crude touch
Test
• Draw a medulla cross section, and label
the Lateral medullary (Wallenberg)
syndrome.
Lateral medullary (Wallenberg) syndrome.
•
Which arteries can result in a
Wallenberg syndrome? Name 4
–
–
–
–
–
Vertebral artery (most common)
PICA
Superior medullary artery
Lateral medullary artery
Middle medullary artery